There is considerable variability in the clinical progression of HIV infection. A number of variables, including a possible defect in the physiological systems mediating coping responses to stressors, are among the hypotheses proposed to explain this variability. Our recent studies showing a blunted norepinephrine response to a cold pressor challenge in HIV+ subjects supports such hypotheses. A major objective of the present proposal is to investigate within an experimentally controlled alpha-and beta-adrenergic challenge paradigm, relationships between autonomic, and HPA axis responses (NE, E, ACTH, Cortisol) that might be related to the stage of HIV-I disease. Furthermore, since relationships among neurohormone, and immune functions have been sufficiently established to permit the advancement of hypotheses relating the role of psychological and behavioral variables in the progression of an immune disease, we also propose to investigate 24-hour urinary NE, E and their metabolites, and cortisol, biological markers of field stressors, as a function of progression of HIV-1 infection. This proposal will examine the responses to evaluative speech, cold pressor and mirror tracing challenges in HIV infection using a cross- sectional design. A group of 90 homosexual subjects (HIV seropositive, CDC stage 1A, 1B, CD4 count greater than 500/cumm, N= 30; HIV+ subjects, CDC stage 2A, 2B, CD4 count 200-500, but no signs of opportunistic infections, N= 30; and HIV-(N= 30) will be enrolled for this study. The responses in the two HIV+ groups and HIV- subjects, will be compared. Also, reactivity results from HIV+ subjects in different stages of the disease will be investigated as a function of CD4 cell counts and other immune markers. The data will be used in determining the role of successful coping with the environmental and acute stressors in the progression of HIV infection. The data may also help in planning behavioral and/or pharmacological interventions designed to normalize coping responses to stressors which may help to delay the progression of HIV-1 infection.